How Does Your Garden Flow? The Impact of Domestic Front Gardens on Urban Flooding.

Aims: To quantify rainwater runoff from domestic front gardens as a consequence of increased impervious surface area and climate change impacts, thus allowing the runoff contribution from both newly and previously covered front gardens to be assessed in terms of the overall urban flood burden. Study Design: Numerical simulation of the runoff from a typical front garden in response to simulated rainfall events for four UK cities (Edinburgh, Manchester, London, and Exeter). Methodology: A typical front garden was simulated with varying areas of impermeable surface area (0%, 10%, 25%, 50%, 75%, and 100%) to represent observed trends in garden paving. Storm events representing current design and projected future rainfall intensities were applied to each of the four cities. The resultant runoff volumes were then quantified. Results: Runoff is shown to be directly proportional to both the impermeable surface area and the rainfall intensity. Areas of impermeable paving can generate substantial volumes of runoff during a storm event which can contribute to localized flooding or add to the urban flood burden. Increased rainfall intensities and frequencies due to climate change are likely to increase runoff further. Conclusion: Domestic front gardens play a vital role in managing surface water runoff in towns and cities. Growing trends of paving over front gardens put this role in jeopardy, while increasing rainfall intensities due to climate change make this role increasingly important. The quantification of domestic front garden runoff provides a mechanism for facilitating the protection, and enhancement, of this important asset in terms of water and urban flood management.

Acute liver failure.

Acute liver failure is a rare but potentially fatal disease. Adult definition of fulminant hepatic failure, which includes the development of hepatic necrosis and encephalopathy within 8 weeks of onset of liver disease does not apply to acute liver failure in children particularly if secondary to autoimmune or metabolic liver disease. The etiology of acute liver failure varies with the age of the child. In neonates, infection or an inborn error of metabolism are common, while viral hepatitis and drug induced liver failure are more likely in older children. The clinical presentation of acute liver failure includes jaundice, coagulopathy and encephalopathy. In neonates, encephalopathy may be subclinical. The management of acute liver failure includes assessment of prognosis for liver transplantation; prevention and treatment of complications while awaiting hepatic regeneration or a donor liver and hepatic support. The major complications of acute liver failure are sepsis, gastro-intestinal bleeding, cerebral edema, renal and cardiac failure. Selection for liver transplantation depends on the etiology of the disease, prognostic factors, the presence or absence of multisystem disease and/or reversible brain damage. Prognostic factors for survival are less well established in children than in adults but children with metabolic liver disease, prothrombin time > 50 seconds, rising bilirubin and falling transaminase, grade II or higher grade of hepatic coma indicate poor prognosis. Most children receive a reduced or split liver graft. Living related donations for acute liver failure are also carried out by some centres. Survival post liver transplantation for acute liver failure has improved and most recipients can expect a 70% five year survival.

Nutrition and growth in patients with chronic liver disease.

Protein energy malnutrition leading to growth failure is an inevitable consequence of chronic liver disease in childhood. Although the precise pathophysiology is not understood considerable progress has been made in understanding the mechanisms of fat malabsorption and protein turnover in liver disease. There are many difficulties with the correct assessment of nutritional parameters in children with liver disease related to their abnormal body composition and energy expenditure and care needs to be taken with the interpretation of results. The effects of malnutrition secondary to chronic liver disease are varied and include fat soluble vitamin deficiencies, generalised growth failure, impairment of gastrointestinal function, immunosuppression and hypotonia. It is now recognised that malnutrition is an important risk factor for liver transplantation and increases both mortality and morbidity. Strategies to prevent or reverse malnutrition are now established and include the use of specific infant formulas based on low salt protein and an increased concentration of medium train triglyceride (50-70%). Careful nutritional support in association with generous fat soluble vitamin supplementation may produce dramatic improvement in catch up weight gain but for those children in whom growth failure persists, the only management is liver transplantation.